Figure 5.

Effect of Skn-1a deficiency on the functional differentiation of Trpm5-positive microvillous cell. (A)In situ hybridization of Trpm5 on coronal sections of the MOE of wild-type and Skn-1a-/- mice. The mRNA signal of Trpm5 was absent in Skn-1a-/- mice. (B and C) Coronal sections of wild-type and Skn-1a-/- MOE of adult mice were immunostained with an anti-Trpm5 antibody (green) and an anti-villin (B) or anti-ChAT (C) antibody (red). Trpm5-positive cells were villin positive in the microvilli in the wild-type MOE (arrowheads), whereas no immunoreactive signal for Trpm5 or villin was observed in the Skn-1a-/- MOE. Trpm5-positive cells were co-immunostained with anti-ChAT antibody in wild-type (arrowheads) but not in Skn-1a-/- mice. Scale bars: 100 μm in A, 10 μm in B and C.

Yamaguchi et al. BMC Neuroscience 2014 15:13   doi:10.1186/1471-2202-15-13
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